Triggering the Autonomic Nervous System

ABSTRACT

A device and method is provided for treating a person by providing controlled stimulation of a branch of the trigeminal nerve of the person to induce a dive reflex response in the person. A device for providing this treatment includes a stimulus component controllably operable to stimulate a branch of the trigeminal nerve of a person. The stimulus component can be a Peltier device configured to reduce the temperature of the person&#39;s face in proximity to a branch of the trigeminal nerve to induce the dive reflex. A controller controls activation of the stimulus component when it is desirable to induce the dive reflex response in the person. The controller can sense physiological and ambient conditions and can activate and deactivate the stimulus component in response to a condition falling within or outside a threshold value.

REFERENCE TO RELATED APPLICATION

This application is a divisional of and claims priority to co-pendingU.S. application Ser. No. 15/138,306, filed on Apr. 26, 2016, which is anon-provisional filing of and claims priority to provisional applicationNo. 62/152,993, filed on Apr. 27, 2015, the entire disclosure of whichis incorporated herein by reference.

BACKGROUND

The present invention relates to medical devices and methods of usingsame, and more particularly to devices and methods for producingbradycardia, increased systemic vascular resistance, decreased cardiacwork, and increased cerebral blood flow through the autonomic nervoussystem in the animal or human body.

The dive reflex, also known as the dive response, is the mechanismthrough which the human body defends itself from hypothermia andresulting death when submerged in cold water. The reflex is mostgraphically illustrated by the resuscitation of children, who have beensubmersed in farm ponds during the winter for periods exceeding thethree-minute brain-death criterion. During the dive reflex, the body,through selective vasoconstriction, isolates those tissues with extendedanaerobic capability from those with relatively little anaerobiccapability, such as the heart and brain. Consequently, circulation tothe extremities is greatly diminished, while circulation to the brainand heart continues at generally adequate or increased levels.Additionally, the pulse-rate slows and a relatively constant bloodpressure is maintained. Typically, the resulting minimum dive-reflexpulse-rate is approximately 60 to 70 percent of the quiescent rate. Byshunting blood to the brain and heart, and slowing the pulse-rate, thebody is able to supply the required oxygen to both the brain and theheart for extended periods of cold water submersion.

Although the dive reflex phenomenon has been known for years, there areseveral new triggering mechanisms for the dive reflex which have onlyrecently been determined. Through selective anatomical immersion, it hasbeen determined that the receptor mechanism is located in the face. See,J. Finley et al, Autonomic Pathways Responsible for Bradycardia onFacial Immersion, Journal of Applied Physiology, Volume 47(6), Pages1218-22 (December 1979). In a 1984, Moore implied in U.S. Pat. No.4,466,439, that the dive reflex was best triggered by isolating andstimulating the seventh cranial facial nerve (Cranial Nerve VII) basedon a hypothesis that the triggering receptor was in the facial nervewhich surfaces at the cheeks, forward of the ears to the nose. This hasnow been disproved and it has since been shown that it is the completelyseparate cranial nerve (fifth cranial nerve V), namely the trigeminalnerve, which possesses the receptors to activate the dive response. Thetrigeminal nerve surfaces over the forehead, between the eyes and downthe upper part of the nose. These receptors in the skin have beenisolated and have been named “cold and menthol” receptors after thestimulus known (at that time) to activate them. Particularly, it is theophthalmic division of the trigeminal nerve which carries this reflex.Further investigations have pointed to the anterior ethmoidal nerve(surfacing on the nose) as being the most capable branch to evoke thisreflex.

Stimulation of the dive response causes bradycardia, reduced cardiacwork, and peripheral vasoconstriction of blood vessels. Blood is removedfrom the limbs and all organs except the heart and the brain allowingthe mammal to conserve oxygen, and shunt blood back to the heart andbrain. In humans, the mammalian dive reflex is not induced when anylimbs are introduced to cold water. Notably, the greatest bradycardiaeffect is induced when the subject is holding one's breath (which maytrigger other mechanoreceptors in the lungs) with the face submerged.This finding may be particularly helpful when utilizing the dive reflexto increase G-force tolerance of military pilots or astronauts.Protocols for the military already include “breath-hold” maneuvers toincrease intra-thoracic pressure (COMBAT EDGE). Further, controversyexists over whether present technologies such as ATAGS (advancedtactical anti G suits) are of any benefit in improving G forcetolerance. Like MAST trousers (now all but obsolete), ATAGS attempts topush fluid and pressure from the lower extremities into the centralvascular tree in an attempt to increase systemic vascular resistance,but no increase in systemic vascular resistance can be documented.Triggering the dive reflex affords the ability to directly access theautonomic nervous system and increase the vascular resistance of everynon-essential vessel throughout the body. Systemic vascular resistanceincreases of 25% have been noted, while increases in the cerebral bloodblow in humans were seen to increase by 14%.

Interestingly, it has also been demonstrated that the spleen, in humans,contracts up to 20% during this reflex to infuse blood and increase thehematocrit up to 5%, thus further improving oxygen delivery to essentialcentral organs. This “auto transfusion” of 5% of oxygen carryingcapacity becomes critical in settings where the individual is losingblood or going into shock. Naturally, with improved hemodynamics andgreater oxygen delivery, cardiac work would be expected to drop and infact this was demonstrated by this investigator to drop by at least 11%using an external monitoring device called impedance plethysmosgraphy(Bio Z monitor).

The present approach to altering the oxygen supply/demand for the heartand brain is to use the 110-year-old technology of a sublingualnitroglycerine tablet or spray that attempts to create the same scenariothrough chemical means. Nitroglycerine works by a mechanism of producingnitric acid inside the vascular wall (thereby dilating it), and itrequires a process of absorption of the chemical (usually through thetongue) taking at least 2 minutes and lasting only 30 minutes. Further,the intent of nitroglycerin action is to improve the oxygen supply anddemand curve of the heart, a goal that is completely in accord with theactions of the dive reflex. Unfortunately, nitroglycerine has not beenable to demonstrate a benefit in the setting of brain attacks (strokesand transient ischemic attacks), whereas, the dive reflex shouldsignificantly prevent or at least improve tolerance of ischemia in thecentral circulation of the brain based on studies which have shown up toa 14% increase in flow to the cerebrum when triggering the dive reflexin humans.

As reported in the Mar. 7, 2002 issue of Nature, McKemy, Neuhausser &Julius characterized and cloned a menthol receptor from trigeminalsensory neurons that is also activated by thermal stimuli in the cool tocold range. This cold- and menthol-sensitive receptor, CMR1, is a memberof the TRP family of excitatory ion channels. They proposed that CMR1functions as a transducer of cold stimuli in the somatosensory system.In February 2004, H-J Behrendt, et. al., published a study on theeffects of 70 odorants and menthol-related substances on recombinantcold-menthol receptor TRPM8 (mTRPM8), expressed in HEK293 cells. Tensubstances (linalool, geraniol, hydroxycitronellal, WS-3, WS-23,FrescolatMGA, FrescolatML, PMD38, CoolactP and Cooling Agent 10) werefound to be agonists.

SUMMARY

The present invention is based on inducing the dive reflex in acontrolled environment in order to specifically alleviate theconsiderable workload of the heart under certain conditions, such asduring post-infarction convalescent periods, or even during anginaevents. This approach does not require the use of sublingualnitroglycerine administration. Such a pulse-rate reduction, underconstant blood pressure (and improved cardiac and cerebral blood flow),would facilitate the recovery of patients due to the reduced requirementfor oxygen by the heart. Additionally, because the blood supply to theextremities is greatly reduced during dive reflex throughvasoconstriction, artificial inducement of the phenomenon could also beused to reduce traumatic bleeding in the extremities (and lessen shock).Moreover, since blood flow is potentiated to the brain, G-induced lossof consciousness (G-loc) in air warriors and astronauts (as well asaltered level of consciousness, A-loc) can be minimized. Lastly, certainconditions can lead to orthostatic hypotension including advanced age,surgical interventions (such as post cardiotomy) and medication use.This mechanism may prevent, or at least improve tolerance and prognosisof, non-hemorrhagic brain attacks, such as strokes and TIA's. Triggeringthe dive reflex on demand in these settings would naturally improve therisks associated with each of the above.

The present invention thus provides a device and method for inducing thedive reflex without the inconvenience of immersing the face in coldwater. The device includes a trigeminal nerve-engaging component, amounting component for mounting the trigeminal nerve-engaging componenton a person's forehead and nose, more particularly over a portion of thearea where the trigeminal nerve surfaces, and a controller operable tocontrol the activation of the trigeminal nerve-engaging component in arange sufficiently to induce the dive reflex through the application ofstimulus to the trigeminal nerve. The method includes the steps ofproviding a device having a stimulus-controllable trigeminalnerve-engaging means, mounting the device on the trigeminal nervedistribution of a person with the trigeminal nerve-engaging meanscovering a portion of the area where the trigeminal nerve surfaces, andcontrolling the stimulus of the trigeminal nerve-engaging means in arange sufficient to induce the dive reflex.

The device and method of the present invention have several medicalapplications. First, the workload on the heart may be reduced byinducing the dive reflex, and associated bradycardia in that patient.Such induced bradycardia is especially beneficial to post-infarctionpatients, and those who may be bradycardial drug resistant. Second,traumatic bleeding in the extremities may be reduced by inducing divereflex, due to the fact that the associated vasoconstriction reduces thevolume of blood circulated through the limbs. Potentiation of cerebralblood flow is of particular importance in settings like G-induced lossof consciousness or altered consciousness, and Brain Attacks (strokesand TIA's).

These and other objects, advantages, and features of the invention willbe more readily understood and appreciated by reference to the writtenspecification and appended drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a depiction of the cutaneous distribution of the trigeminalnerve in a human.

FIG. 2 is a depiction of the anterior ethmoidal nerve of the trigeminalnerve.

FIG. 3 is a depiction of the reflex pathway for the Mammalian divereflex as it interacts with the autonomic nervous system.

FIG. 4 is a view of the underside of a device helmet incorporating aplurality of stimulus components operable to stimulate the dive reflexin a person.

FIG. 5 is a perspective view of a Peltier device for use with the deviceshown in FIG. 4.

FIG. 6 is a view of the underside of a device helmet incorporating aplurality of stimulus components in the form of radiator coolingelements for use by an aviator.

FIG. 7 is a cross-sectional representation of a patch including stimuluscomponents for triggering the dive reflex in a person upon applicationof the patch.

DETAILED DESCRIPTION

For the purposes of promoting an understanding of the principles of thedisclosure, reference will now be made to the embodiments illustrated inthe drawings and described in the following written specification. It isunderstood that no limitation to the scope of the disclosure is therebyintended. It is further understood that the present disclosure includesany alterations and modifications to the illustrated embodiments andincludes further applications of the principles disclosed herein aswould normally occur to one skilled in the art to which this disclosurepertains

The portions of the ophthalmic distribution of the human trigeminalnerve that are capable of triggering the parasympathetic nervous systempertinent to dive reflex are illustrated in FIG. 1. By way oforientation, the top portion of the diagram illustrates the ophthalmicbrand which includes the entire forehead and top of the cranium, theeyes, part of the temples, the bridge of the nose and down to the tip ofthe nose. It is this portion of the trigeminal nerve that is of mostinterest in stimulating the dive response.

More specifically, the anterior ethmoidal nerve branch is believed toelicit the mammalian dive reflex stronger than in the other trigeminalbranches. As shown in the diagram of FIG. 2, the ethmoidal nerve coursesalongside the nose to surface to the skin just on either side of thebridge of the nose. The vagus nerve leads from the brain (not shown)through the head and neck and into the thoracic cavity. General visceralefferent fibers extend from the vagus nerve and surface in the heart tocontrol the heart and its pulse-rate. The trigeminal nerve, vagus nerveand general visceral efferent fibers serve as the autonomic pathwaythrough which the dive reflex is activated, as depicted in FIG. 3. Itcan be seen that the trigeminal receptors and the tele-receptors act onthe cortical and hypothalamic centers which in turn act on therespiratory, the cardio (acceleratory and inhibitory centers), and thevasomotor centers.

When a triggering stimulus is applied to at least a portion of area inwhich the trigeminal nerve surfaces, the parasympathetic nervous systemis triggered and slows the heartbeat by communicating with heart throughthe vagus nerve, and general visceral efferent fibers. Maximum heartbeatreduction is estimated to be 60 percent. The parasympathetic nervoussystem also causes vasoconstriction and its associated reduction incirculation to those body extremities and other organs thus extendinganaerobic capability. Accordingly, the dive reflex can be selectivelyinduced by applying a carefully controlled triggering source to theophthalmic area depicted.

According to one aspect of the present invention, a device 10 isprovided for inducing the dive reflex in the person, as illustrated FIG.4. In accordance with this embodiment, the device 10 includes a headgear component 12 that is configured to be worn by the person. The headgear component can include a helmet 13, as shown, or may incorporateother structure adapted to be worn by the person. The head gearcomponent includes a face-engaging plate 15 that is arranged toencompass the ophthalmic zone of the trigeminal nerve of the person,particularly at a location where the trigeminal nerve approaches thesurface of the skin, and more particularly to be in proximity to thelocation of the anterior ethmoidal nerve. In the illustrated embodiment,the face-engaging plate is in the form of a bar that is adjustablymounted to the helmet 13 so that the interior surface 16 of the bar canbear against the skin of the person. The interior of the bar 15 isprovided with padding 18 for the comfort of the person. In lieu of ahelmet, the device may have a structure similar to a conventional CPAPmask in which the mask is replaced with the face-engaging bar 15. It iscontemplated that the head gear component 12 and particularly theface-engaging bar 15, may be formed of a moldable material that can beshaped to tightly conform to the anatomy of the person's face, andparticularly to provide a snug fit on the bridge of the person's nosewhere the relevant branches of the trigeminal nerve are found.

The device 10 further includes a mechanism for stimulating the ethmoidalnerve in the form of a plurality of stimulus components 20 a-c embeddedwithin the padding 18 but near the interior surface 16 to maximize theeffect of the stimulus produced by the components 20 a-c. The stimuluscomponents may be integrated into the padding or may be placed inpockets formed in the padding to permit ready removal and replacement ofthe stimulus components. The plurality of components 20 are distributedon the face-engaging bar 15 so that a component is positioned inimmediate proximity to a branch of the trigeminal nerve. For instance,in the embodiment shown in FIG. 4, three components 20 are provided,with two components 20 a, 20 b positioned on either side of the person'snose in immediate proximity to the anterior ethmoidal nerve and a thirdcomponent 20 c centrally located in proximity to the infracochlearnerve.

The stimulus components 20 a-c are devices operable to simulate theapplication of cold water to the person's face. Thus, in one specificembodiment, the components 20 a-c are thermoelectric cooling (TEC)devices, such as the Peltier device 25 shown in FIG. 5. As known in theart, a typical Peltier device includes two unique semiconductors withdifferent electron densities. The semiconductors are placed thermally inparallel to each other and electrically in series and then joined with athermally conducting plate on each side. When a voltage is applied tothe free ends of the two semiconductors there is a flow of DC currentacross the junction of the semiconductors causing a temperaturedifference. The side with the cooling plate absorbs heat which is thenmoved to a heat sink on the other side of the device. The device 10, andparticularly the face-engaging bar 15, includes a heat sink panel 22that serves as the heat sink for the Peltier devices 20 a-c. The heatsink panel 22 is operable to draw heat away from the Peltier devices andconvey the heat to other parts of the helmet 12. A Peltier device, suchas device 25, is suitable for use as the stimulus components 20 a-cbecause the can be provided in a minimal envelop, typically having athickness of 15-25 mil.

The device 10 further includes a controller 30 that can incorporate apower supply or a mating connector for engagement to an external powersupply. The controller 30 includes circuitry and electronics to controlthe activation of the stimulus components 20 a-c. The controller 30 maythus be application specific, meaning that the manner and degree ofcontrol of the stimulus components depends upon the purpose of invokingthe dive reflex in the person. For instance, if the device 10 is to beused as part of a pain management, palliative care or critical careregimen, the controller 30 can require manual external activation andde-activation. The controller 30 may include condition sensors, such asdermal temperature or heart rate sensors, to provide further control ofthe activation and de-activation of the stimulus components. Forinstance, the controller can be operable to de-activate the stimuluscomponents when the skin temperature drops to a pre-determinetemperature. Other sensors, such as bio-sensors like cardiac and brainwave monitors, may provide signals to the controller and the controllermay incorporate appropriate electronics and/or software to control theoperation of the stimulus components. The stimulus components 20 a-c andthe controller 30 may be configured to produce and maintain atemperature in a range of approximately 35° to 60° F. for a desired timeperiod.

Another application of the device 10 is to offset the effect of G-forceson an aviator. With this application, the controller 30 may beconfigured to interface with the avionics on an aircraft allowing forsynchronized activation of the stimulus components 20 a-c upon receiptof information that a pre-determined level of G-forces are beingapplied. When the G-forces fall below the pre-determined level thecontroller 30 can deactivate the stimulus components. It can beappreciated that the activation of the diving reflex during high G-forcemaneuvers would help the aviator better tolerate the G-forces withoutlosing consciousness or suffering from reduced awareness. In thisparticular application, the helmet 12 can be the aviator's standardhelmet with the stimulus components 20 a-c and controller 30 integratedinto the helmet. In this embodiment, the controller 30 may be driven bythe avionics, as described, and/or may require manual activation of theaviator. In this latter case, the stimulus components may be activatedby the aviator to provide cooling to the aviator's head.

The controller 30 on-board the device 10 may incorporate the powersupply or power supply access and may itself have limited functionality.In this embodiment, the controller 30 includes a component forcommunication with an external controller. The component may be anelectrical input for a hard-wired connection to an external device, suchas a laptop computer. Alternatively, the component may be operable toprovide a wireless communication link with the external device, such asan IR, Bluetooth or wireless communication link. The external devicecould be a “smart” device, such as a smart phone or smart pad, whichoperates a software app to control the operation of the controller 30and ultimately the stimulus components 20 a-c. The software or appexecuted by the external device can be tailored to the specificapplication for invoking the dive reflex response.

The present invention contemplates other forms of stimulus componentsthat are capable of stimulating the trigeminal nerve to invoke the divereflex response. In one embodiment, stimulus components 40 a-c may be inthe form of radiator elements mounted in a helmet 41 that are connectedto an external source of cool or cold air. In an aircraft, the externalsource can be ambient air diverted through a pitot tube outside theaircraft into a delivery hose 42 inside the aircraft for connection tothe device 10. The delivery hose 42 may incorporate a heating element 43to warm the incoming ambient air (which can be 20-30° F. below zero)prior to introduction into the stimulus components 40 a-c. Cold air flowthrough the delivery hose 42 into the radiator elements 20 a-c provideconvection cooling to the person at the trigeminal nerve to stimulatethe dive reflex. In this embodiment, a controller 44 is provided thatcontrols a flow regulator valve integrated into the helmet 13 or intothe controller, with the nature of the control depending on whether theneed for dive reflex stimulation is indicated or whether the device 10is being used simply as a cooler for the aviator. The controller 44 mayalso be configured to control the heating element 43, particularly whenthe stimulus components are being used by the aviator as an internalcooling system. The delivery hose may incorporate a discharge hose orthe helmet 41 may be provided with vents to vent the air stream outsideor inside the helmet.

In the above embodiments, the trigeminal nerve is stimulated by theapplication of extreme cold to the person's face, thereby activating thenerve and the dive response. In an alternative approach, the trigeminalnerve may be directly stimulated by application of a small electricalcurrent to the surface of the skin. With this approach, the stimuluscomponents 20 a-c described above are replaced with an electricalstimulus device that is held in direct contact with the person's skin atthe location of the trigeminal nerve branches of interest. Theelectrical stimulus devices can be TENS units (Transcutaneous ElectricalNerve Stimulators), Micro-TENS units, pulsed galvanic stimulators,interferential stimulators, or muscle stimulators. In this embodiment,the controller 30 may include a power supply and a controllabletransformer to power the electrical stimulus devices. The controller 30may be operable at several settings to control the electrical currentprovided to the electrical stimulus devices to achieve a maximal ordesired result.

As a further alternative, the electrical stimulus components may beself-powered, meaning that a separate power supply is not required. Inthis alternative, the electrical stimulus components may be in the formof a battery cell that is activated when desired. The battery cell maybe a chemical battery embedded into a conductive patch supported by thehead gear component, such as component 12. A controller, such as thecontroller 30, is operable to activate the battery cell which thengenerates an electrical signal applied to the skin through theconductive patch to thereby activate the trigeminal nerve.

As described above, the face-engaging bar 18 may be provided withpockets for holding the stimulus components 20 a-c. In a furtherembodiment, the stimulus components may be activated independently ofthe device 10 and then placed in a corresponding pocket. The user donsthe head gear component 12 so that the stimulus components are incontact with the use's face, as described above. In this embodiment, thestimulus components are patches, such as patch 50 show in FIG. 7, thatcontain a composition that operates as a cold receptor agonist capableof stimulating the dive reflex. The composition may be a salve, lotion,cream or emollient, or other flowable composition. The patch 50 includesa body 52 that defines a reservoir 51 for the composition. The reservoir51 communicates with a permeable membrane 54 that is held in contactwith the use's skin by the face-engaging bar 18. The patch 50 may beprovided with a releasable liner (not shown) initially covering thepermeable membrane 54. For use, the liner is removed, the patches 50 areplaced within the pockets in the face-engaging bar 18 at the positions20 a-c (FIG. 4) and the head gear component is placed on the user'shead. The composition immediately flows through the membrane intocontact with the skin, thereby prompting a reaction of the trigeminalnerve and invocation of the dive reflex. The salve, lotion, cream oremollient can be menthol, menthol derivative, menthol receptor agonists(linalool, geraniol, hydroxycitronellal, WS-3, WS-23, FrescolatMGA,FrescolatML, PMD38, CoolactP and Cooling Agent 10), or other coldreceptor agonists.

In an alternative, the salve or lotion within the patch 50 may be anactivatable composition including at least two substances initiallycontained within separate reservoirs in the patch. The composition isactivated by rupturing a wall between the two compartments, therebyallowing the substances to mix. Upon mixing, the composition produces anendothermic reaction reducing the temperature of the patch and thus thedermal interface to a desired temperature that is sufficient to initiatethe dive reflex, such as 35-40° F. Two suitable components are urea andwater, which in a 50:50 mixture will reduce the patch temperature toabout 35° F. for about three hours. Different temperatures and durationscan be obtained with different ratios of urea and water. It can beappreciated that in this alternative embodiment the stimulus componentsare single use, meaning that once the composition has been activated tocreate the endothermic reaction the reaction will continue unabateduntil the chemical reaction is complete, after which the composition isinert.

In this alternative as just described, the patch 50 is held withinpockets in the head gear component 12. Alternatively, the patch 50, andparticularly the body 52, may be formed in a shape to conform to thebridge of a person's nose. The body 52 may also be slightly moldablefrom this initial conforming shape so that the body can be preciselymolded to the particular user's anatomy. The body 52 around thepermeable membrane or the permeable membrane 54 can be provided with anadherent or tacky layer that is adapted for removable adhesion to aperson's skin. Suitable tacky layers can include hydrocolloid adhesives,acrylate adhesives, polybutene, resin tackifiers or other knownmaterial. As a modification of the steps described above, once theinternal components have been activated to initiate the endothermicreaction, the body 52 of the patch 50 is pressed onto the bridge of theuser's nose. The patch can be readily removed once the reaction iscomplete or as desired by the user. It can be appreciated that thesalve/lotion embodiment discussed above could also be implemented in asimilar manner.

In a further aspect of the invention, a method is provided for improvingthe outcome of a soldier or patient in the setting of shock, impendingshock, fainting, or profound blood loss. Historically, MAST (militaryanti shock trousers) have been utilized with the intent to increase thesystemic vascular resistance of the wearer to afford them greaterprotection against drops in blood pressure or shifts of blood away fromthe center axis of the brain and heart. Unfortunately, these devicesfell out of favor in the 1990's due to their inability to actuallysustain any increase in SVR (systemic vascular resistance). As the MASTwas inflated approximately 900 ccs of blood was pushed into the centralcirculation and the strike volume of the heart increased.Counter-regulatory actions of the heart provide for the reflex mechanismof a drop in SVR to counter the sudden increased stroke volume and theintended benefit was quickly lost. The triggering of the dive reflexaffords a mechanism whereby the entire autonomic nervous system workstogether to create an increase in SVR (on the order of 25%) with asecondary drop in cardiac work and a surprising increase in cerebralblood flow. The present invention provides a device capable oftriggering the dive reflex on demand, which can get an injured orbleeding soldier through the so-called “Golden Hour” where he/she needsto be transferred to acute care before death or irreversible injuryoccurs. Even in the field, a soldier who just sustained a round orshrapnel to a vein or artery may be able to activate the present deviceto trigger the dive reflex thereby staying conscious long enough to fendoff further attacks or to signal for help. Even the setting where abullet may have impaled a major internal structure such as the liver oreven the spleen, would be benefited by triggering the dive reflex wherethe spleen is known to contract by as much as 20% upon activating thedive reflex and the hematocrit or blood volume may go up as much as 10%upon contracture of the spleen. Oxygen carrying capacity to vital organsis not only preserved but may actually be increased to the criticalorgans of heart and brain at this life threatening juncture. Inaccordance with this aspect of the invention, the soldier's helmet isequipped in the manner of the helmet 10 described above. The controller30 may be equipped with a manually activatable switch that allows thesoldier to activate the stimulus components 20 a-c in the event of atrauma. Alternatively, the controller 30 may be equipped with sensorsthat continuously monitor the soldier's vital signs and is calibrated toautomatically activate the stimulus components when the vital signssignal the onset of a trauma.

In a further aspect, the device and method of the present invention canbe implemented to trigger the dive reflex in a person with the intent toimprove the oxygen supply/demand curve to the heart or brain. The100-year-old sublingual nitroglycerine tablet works by a very simple andwell defined mechanism. The nitroglycerine is absorbed through the oralmucosa and circulates to the endothelial lining of the arteries andveins of the system. In the vessel lining, the nitroglycerin isconverted to nitric oxide, a known vasodilator. The venous system isactually dilated greater than the arterial system (which is generallynot an advantageous), but the reduced flow into the heart (by dilatingthe veins) appears to reduce oxygen demand by the heart so that the riskof angina or congestive heart failure is reduced. Activation of the divereflex in the person can impart an even greater theoretical benefit tothe vascular tree, especially to the heart and brain. Just as in thesublingual nitroglycerine, the oxygen demand (cardiac work) has beendemonstrated to drop by more than 10%. Moreover, unlike nitroglycerine,the dive reflex shunts oxygen rich blood away from non-essentialperipheral organs back to the heart and brain. Further, the dive reflexhas been demonstrated to actually increase cerebral blood flow, whichhas not shown in the use of nitroglycerine. The spleen has been shown tocontract upon triggering the dive response which serves to increase thehematocrit (volume of blood) to bolster the oxygen carrying capacity ofthe blood stream thereby benefiting the heart and brain. Nitroglycerinehas been known to cause an unfavorable reflexive increase in heart rate(tachyphylaxis) that is injurious to the oxygen starved heart. On theother hand, the dive reflex causes bradycardia (20-70% drop) which isgenerally preferable to the tachyphylaxis caused by nitroglycerine.Furthermore, sublingual nitroglycerine is known to take 2-4 minutes toact, last only 25-30 minutes, often result in tolerance to the drug, andoften result in severe headaches. The triggering of the dive reflexwould not be expected to result in any of these side effects. Thus, inaccordance with this method of the invention, a person in need ofincreased oxygen supply to the heart and brain is fitted with a helmet,such as the helmet 10, and the stimulus components 20 a-c are activatedto produce the dive reflex response in the person. A less intrusive headgear component, such as the CPAP-type component described above, may beused, or an individually applied patch, such as the patch 50 may beused.

In a similar manner the devices disclosed herein can be used to triggerthe dive reflex in a person with the intent to mitigate or preventmigraine headaches. Migraines are known to be caused by a spasm of thecerebral vessels with resulting vasodilatation leading to painthereafter. If the patient were able to trigger the dive refleximmediately upon recognizing the premonitory signs (visual symptoms,tunnel vision, altered taste, smell, numbness for example), then theymay be able to abort the headache before it starts. The person may don ahelmet, such as the helmet 10 shown in FIG. 4, or a less obtrusive headgear component 12, such as the CPAP mask-type component. Alternatively,the person may apply the patch 50 shown in FIG. 7.

The devices disclosed herein may further be used to initiate the divereflex with the intent to improve the medical condition known as brainattacks also known as strokes, RINDS (reversible ischemic neurologicaldeficits) or TIAS (transient ischemic attacks). Certainly, there may bea contraindication to triggering the dive reflex if a neurological eventwere to be secondary to a hemorrhagic event. Further, since it may notbe obvious whether an event is hemorrhagic or not, an imaging proceduremay be required before initiating the dive reflex in the stated setting.Similarly, the dive reflex can be triggered with the intent to improvethe hypotension associated with medical conditions such as Shy-Dragar'sSyndrome, Holmes-Adie syndrome, autonomic neuropathy from diabetes orany cause, orthostatic hypotension from drugs or prior strokes, or fromany hypotensive cause. In these settings the dive reflex can betriggered on demand to allow the individual a temporary reprieve fromthe orthostatic drop in blood pressure experienced. As with thepreviously-described methods, any of the devices disclosed herein may beimplemented to activate the dive reflex in the patient.

The present disclosure should be considered as illustrative and notrestrictive in character. It is understood that only certain embodimentshave been presented and that all changes, modifications and furtherapplications that come within the spirit of the disclosure are desiredto be protected. For instance, the devices and methods described hereinmay be used to trigger the dive reflex response in a person to addressany of the following medical conditions, as well as other similarconditions:

-   -   (a) to improve the blood flow to the brain during a fainting        spell, migraine headache attack, cluster headache attack, panic        attacks, or even a seizure;    -   (b) to improve the outcome of brain surgery or cardiothoracic        surgery outcomes;    -   (c) to improve known hypotensive conditions such as Shy-Dragar's        Syndrome, Holmes-Adie syndrome, autonomic neuropathy from        diabetes or any cause, orthostatic hypotension from drugs or        prior strokes, or from any cause;    -   (d) to improve any tachycardia rhythm of the heart or even        convert supraventricular tachycardia (SVT) or paroxysmal SVT to        normal sinus rhythm when it occurs as an outpatient or when the        patient presents to the Emergency Medical System (EMT,        Paramedic, Medic, or Emergency Room). Such rhythms include but        are not limited to atrial fibrillation, Wolf-Parkinson-White        Syndrome (WPW), AVNRT (AV nodal reentrant tachycardia), AVRT (AV        reentrant tachycardia), or Junctional Tachycardia;    -   (e) to improve cardiac and cerebral outcomes after any surgery        where anesthesia is administered. Anesthesia can lead to carotid        baroreceptor dysfunction that could be benefited by the dive        reflex;    -   (f) to improve survival technique when one is lost in the snow,        lake or ocean water, or even just wilderness exposure waiting to        be found. Extending the victim's survival time would improve the        likelihood of search teams locating the victim;    -   (g) to improve the tolerance of hypoxia (lack of oxygen) during        sleep apnea or other altered sleeping patterns. Sleep apnea is        known to adversely alter the autonomic nervous system and even        trigger high blood pressure in more than half of patients with        the disorder. Reducing cardiac demand and oxygen consumption        would benefit the individual greatly. Use, in conjunction with        CPAP (Continuous Positive Airway Pressure), would further        augment the actions of the dive response as triggering        mechanoreceptors in the lungs (such as with breath holding) has        shown even greater dive response activation;    -   (h) to improve a palpitations condition whereby the heart is        summoned to beat too early in its cycle and the dive reflex        could slow, stop or prevent such an action.

What is claimed is:
 1. A device for inducing the dive reflex in a personcomprising: at least one stimulus component operable to stimulate abranch of the trigeminal nerve of the person in a manner sufficient toinduce a dive reflex response in the person; and an apparatus forsupporting the at least one stimulus component in contact with theperson's face directly adjacent a branch of the trigeminal nerve.
 2. Thedevice of claim 1, wherein: the apparatus is a patch configured toconform to the person's face about the nose in proximity to a branch ofthe trigeminal nerve of the person, the patch including; a body defininga reservoir; a permeable membrane; and an adherent layer adapted toremovably adhere to the skin of the person; and the at least onestimulus component includes a composition adapted to pass through thepermeable membrane into contact with the person's skin and is adapted tostimulate the trigeminal nerve to activate the dive reflex in theperson.
 3. The device of claim 2, wherein the patch is configured toconform to the person's face about the bridge of the nose in proximityto the anterior ethmoidal nerve of the person.
 4. The device of claim 2,wherein the composition is a cold receptor agonist.
 5. The device ofclaim 4, wherein the composition includes menthol, a menthol derivativeor a menthol receptor agonist, such as linalool, geraniol,hydroxycitronellal, WS-3, WS-23, FrescolatMGA, FrescolatML, PMD38,CoolactP and Cooling Agent
 10. 6. The device of claim 1, wherein theapparatus includes a head gear component adapted to be worn on the headof the person and including a face-engaging plate supporting the atleast one stimulus component in direct contact with the face of theperson directly adjacent a branch of the trigeminal nerve.
 7. The deviceof claim 1, wherein the at least one stimulating component includes aPeltier device operable to reduce the temperature of the person's skinwhen in contact with the person's face directly adjacent a branch of thetrigeminal nerve.
 8. The device of claim 7, wherein the apparatusincludes a head gear component adapted to be worn on the head of theperson and including a face-engaging plate defining at least one pocketconfigured to receive a corresponding one of the at least one stimuluscomponent in direct contact with the face of the person directlyadjacent a branch of the trigeminal nerve.
 9. The device of claim 8,wherein the face-engaging plate includes a heat sink panel in contactwith each Peltier device of each of the at least one stimulus componenton a surface of the Peltier device opposite the skin of the person. 10.The device of claim 1, further comprising a controller supported on theapparatus and operably connected to the at least one stimulus componentto activate the stimulus component to stimulate a branch of thetrigeminal nerve of the person directly adjacent the stimulus component.11. The device of claim 10, wherein: the at least one stimulatingcomponent includes a Peltier device operable to reduce the temperatureof the person's skin when in contact with the person's face directlyadjacent a branch of the trigeminal nerve; and said controller includesa power supply for providing electrical power to the Peltier device. 12.The device of claim 10, wherein: the at least one stimulus component iscontrollable to maintain a predetermined temperature of the person'sskin when in contact with the person's face; and the controller isconfigured to control the at least one stimulus apparatus to maintainthe predetermined temperature.
 13. The device of claim 12, wherein theat least one stimulus component is operable to maintain a temperature inthe range of 35-60° F.
 14. The device of claim 10, wherein thecontroller is connected to one or more sensors configured to sense aphysiological or ambient condition of the person and is operable toactivate the at least one stimulus component when a sensed condition isoutside a threshold value.
 15. The device of claim 14, wherein theambient condition is the G-force experienced by the person and thethreshold value is a G-force value at which the person experiencesreduced awareness or loss of consciousness.
 16. The device of claim 14,wherein the controller is configured to de-activate the at least onestimulus component when a sensed condition is within a threshold value.17. The device of claim 1, wherein the at least one stimulus componentincludes a component for applying an electrical current to the person'sface.
 18. The device of claim 17, wherein the component is atranscutaneous electrical nerve stimulator (TENS) device.